First Author | Zhang B | Year | 2015 |
Journal | Cell Rep | Volume | 11 |
Issue | 5 | Pages | 715-26 |
PubMed ID | 25921526 | Mgi Jnum | J:228367 |
Mgi Id | MGI:5706867 | Doi | 10.1016/j.celrep.2015.03.059 |
Citation | Zhang B, et al. (2015) An oncogenic role for alternative NF-kappaB signaling in DLBCL revealed upon deregulated BCL6 expression. Cell Rep 11(5):715-26 |
abstractText | Diffuse large B cell lymphoma (DLBCL) is a complex disease comprising diverse subtypes and genetic profiles. Possibly because of the prevalence of genetic alterations activating canonical NF-kappaB activity, a role for oncogenic lesions that activate the alternative NF-kappaB pathway in DLBCL has remained elusive. Here, we show that deletion/mutation of TRAF3, a negative regulator of the alternative NF-kappaB pathway, occurs in approximately 15% of DLBCLs and that it often coexists with BCL6 translocation, which prevents terminal B cell differentiation. Accordingly, in a mouse model constitutive activation of the alternative NF-kappaB pathway cooperates with BCL6 deregulation in DLBCL development. This work demonstrates a key oncogenic role for the alternative NF-kappaB pathway in DLBCL development. |